The Effect of GADD45a on Furazolidone-Induced S-Phase Cell-Cycle Arrest in Human Hepatoma G2 Cells

2015 ◽  
Vol 29 (10) ◽  
pp. 489-495 ◽  
Author(s):  
Yu Sun ◽  
Shusheng Tang ◽  
Xilong Xiao
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
S Phase ◽  
Phase Cell ◽  
Human Hepatoma ◽  
Cycle Arrest ◽  
G2 Cells

Involvement of the p38 MAPK signaling pathway in S-phase cell-cycle arrest induced by Furazolidone in human hepatoma G2 cells

2012 ◽  
Vol 33 (12) ◽  
pp. 1500-1505 ◽  
Author(s):  
Yu Sun ◽  
Shusheng Tang ◽  
Xi Jin ◽  
Chaoming Zhang ◽  
Wenxia Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
S Phase ◽  
Mapk Signaling Pathway ◽  
Phase Cell ◽  
Human Hepatoma ◽  
Cycle Arrest

Ciprofloxacin-mediated induction of S-phase cell cycle arrest and apoptosis in COLO829 melanoma cells

2018 ◽  
Vol 70 (1) ◽  
pp. 6-13 ◽  
Author(s):  
Artur Beberok ◽  
Dorota Wrześniok ◽  
Aldona Minecka ◽  
Jakub Rok ◽  
Marcin Delijewski ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Melanoma Cells ◽  
S Phase ◽  
Phase Cell ◽  
Cycle Arrest

scholarly journals Potent organometallic osmium compounds induce mitochondria-mediated apoptosis and S-phase cell cycle arrest in A549 non-small cell lung cancer cells

Metallomics ◽  
2014 ◽  
Vol 6 (5) ◽  
pp. 1014 ◽  
Author(s):  
Sabine H. van Rijt ◽  
Isolda Romero-Canelón ◽  
Ying Fu ◽  
Steve D. Shnyder ◽  
Peter J. Sadler
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Small Cell ◽  
S Phase ◽  
Phase Cell ◽  
Small Cell Lung ◽  
Cycle Arrest

Furazolidone induced oxidative DNA damage via up-regulating ROS that caused cell cycle arrest in human hepatoma G2 cells

2011 ◽  
Vol 201 (3) ◽  
pp. 205-212 ◽  
Author(s):  
Xi Jin ◽  
Shusheng Tang ◽  
Qian Chen ◽  
Jiajie Zou ◽  
Ting Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Oxidative Dna Damage ◽  
Human Hepatoma ◽  
Cycle Arrest ◽  
G2 Cells

scholarly journals Cannabisin B induces autophagic cell death by inhibiting the AKT/mTOR pathway and S phase cell cycle arrest in HepG2 cells

2013 ◽  
Vol 138 (2-3) ◽  
pp. 1034-1041 ◽  
Author(s):  
Tianpeng Chen ◽  
Jianxiong Hao ◽  
Jinfeng He ◽  
Jianchun Zhang ◽  
Yingcong Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
S Phase ◽  
Mtor Pathway ◽  
Autophagic Cell Death ◽  
Phase Cell ◽  
Cycle Arrest

scholarly journals Ghrelin enhances cisplatin sensitivity in HO-8910 PM human ovarian cancer cells

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yun Leng ◽  
Can Zhao ◽  
Guoliang Yan ◽  
Shuangyue Xu ◽  
Yinggui Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Cycle Arrest ◽  
Cyclin B1 ◽  
Inhibitory Effect ◽  
S Phase ◽  
Phase Cell ◽  
Ovarian Cancer Cells ◽  
Cycle Arrest

Abstract Background Resistance to platinum-based chemotherapy is one of the crucial problems in ovarian cancer treatment. Ghrelin, a widely distributed peptide hormone, participates in a series of cancer progression. The aim of this study is to determine whether ghrelin influences the sensitivity of ovarian cancer to cisplatin, and to demonstrate the underlying mechanism. Methods The anti-tumor effects of ghrelin and cisplatin were evaluated with human ovarian cancer cells HO-8910 PM in vitro or in vivo. Cell apoptosis and cell cycle were analyzed via flow cytometry assay. The signaling pathway and the expression of cell cycle protein were analyzed with Western Blot. Results Our results showed that treatment with ghrelin specifically inhibited cell proliferation of HO-8910 PM and sensitized these cells to cisplatin via S phase cell cycle arrest, and enhanced the inhibitory effect of cisplatin on tumor growth of HO-8910 PM derived xenografts in vivo. Treatment with ghrelin inhibited the expression of p-Erk1/2 and p-p38, which was opposite the effect of cisplatin. However, under the treatment of ghrelin, cisplatin treatment exhibited a stronger effect on inhibiting P21 expression, upregulating p-CDK1 and cyclin B1 expression, and blocking cell cycle progression. Mechanistically, ghrelin promoted S phase cell cycle arrest and upregulated p-CDK1 and cyclin B1 expression induced by cisplatin via inhibition of p38. Conclusion This study revealed a specifically inhibitory effect of ghrelin on platinum-resistance via suppressing p-P38 and subsequently promoting p-CDK1 mediated cell cycle arrest in HO-8910 PM.

scholarly journals Legionella pneumophila translocated translation inhibitors are required for bacterial-induced host cell cycle arrest

2019 ◽  
Vol 116 (8) ◽  
pp. 3221-3228 ◽  
Author(s):  
Asaf Sol ◽  
Erion Lipo ◽  
Dennise A. de Jesús-Díaz ◽  
Connor Murphy ◽  
Mildred Devereux ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Host Cell ◽  
Legionella Pneumophila ◽  
S Phase ◽  
Phase Cell ◽  
Cycle Arrest ◽  
Bacterial Replication ◽  
Cell Cycle Machinery

The cell cycle machinery controls diverse cellular pathways and is tightly regulated. Misregulation of cell division plays a central role in the pathogenesis of many disease processes. Various microbial pathogens interfere with the cell cycle machinery to promote host cell colonization. Although cell cycle modulation is a common theme among pathogens, the role this interference plays in promoting diseases is unclear. Previously, we demonstrated that the G1 and G2/M phases of the host cell cycle are permissive for Legionella pneumophila replication, whereas S phase provides a toxic environment for bacterial replication. In this study, we show that L. pneumophila avoids host S phase by blocking host DNA synthesis and preventing cell cycle progression into S phase. Cell cycle arrest upon Legionella contact is dependent on the Icm/Dot secretion system. In particular, we found that cell cycle arrest is dependent on the intact enzymatic activity of translocated substrates that inhibits host translation. Moreover, we show that, early in infection, the presence of these translation inhibitors is crucial to induce the degradation of the master regulator cyclin D1. Our results demonstrate that the bacterial effectors that inhibit translation are associated with preventing entry of host cells into a phase associated with restriction of L. pneumophila. Furthermore, control of cyclin D1 may be a common strategy used by intracellular pathogens to manipulate the host cell cycle and promote bacterial replication.

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